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Neurol Clin. 2008 May ; 26(2): 521–541.
Management of Intracranial Hypertension
Leonardo Rangel-Castillo, MD, Shankar Gopinath, MD, and Claudia S. Robertson, MD*
Department of Neurosurgery, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030,
USA
Abstract
Effective management of intracranial hypertension involves meticulous avoidance of factors that
precipitate or aggravate increased intracranial pressure. When intracranial pressure becomes
elevated, it is important to rule out new mass lesions that should be surgically evacuated. Medical
management of increased intracranial pressure should include sedation, drainage of cerebrospinal
fluid, and osmotherapy with either mannitol or hypertonic saline. For intracranial hypertension
refractory to initial medical management, barbiturate coma, hypothermia, or decompressive
craniectomy should be considered. Steroids are not indicated and may be harmful in the treatment
of intracranial hypertension resulting from traumatic brain injury.
Intracranial hypertension is a common neurologic complication in critically ill patients; it is

the common pathway in the presentation of many neurologic and non-neurologic disorders.
The underlying pathophysiology of increased intracranial pressure (ICP) is the subject of
intense basic and clinical research, which has led to advances in understanding of the
physiology related to ICP. Few specific treatment options for intracranial hypertension have
been subjected to randomized trials, however, and most management recommendations are
based on clinical experience.
Intracranial pressure
Normal values
In normal individuals with closed cranial fontanelles, central nervous system contents,
including brain, spinal cord, blood, and cerebrospinal fluid (CSF), are encased in a
noncompliant skull and vertebral canal, constituting a nearly incompressible system. There is
a small amount of capacitance in the system provided by the intervertebral spaces. In the
average adult, the skull encloses a total volume of 1450 mL: 1300 mL of brain, 65 mL of CSF,
and 110 mL of blood [1]. The Monroe-Kellie hypothesis states the sum of the intracranial
volumes of blood, brain, CSF, and other components is constant, and that an increase in any
one of these must be offset by an equal decrease in another, or else pressure increases. An
increase in pressure caused by an expanding intracranial volume is distributed evenly
throughout the intracranial cavity [2,3].
*Corresponding author. E-mail address: claudiar@bcm.tmc.edu (C.S. Robertson).

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Rangel-Castillo et al. Page 2
The normal range for ICP varies with age. Values for pediatric subjects are not as well
established. Normal values are less than 10 to 15 mm Hg for adults and older children, 3 to 7
mm Hg for young children, and 1.5 to 6 mm Hg for term infants. ICP can be subatmospheric
in newborns [4]. For the purpose of this article, normal adult ICP is defined as 5 to 15 mm Hg
(7.5–20 cm H2O). ICP values of 20 to 30 mm Hg represent mild intracranial hypertension;
however, when a temporal mass lesion is present, herniation can occur with ICP values less
than 20 mm Hg [5]. ICP values greater than 20 to 25 mm Hg require treatment in most
circumstances. Sustained ICP values of greater than 40 mm Hg indicate severe, life-threatening
intracranial hypertension.
Cerebral dynamics overview

Cerebral perfusion pressure (CPP) depends on mean systemic arterial pressure (MAP) and ICP
by the following relationship:
As a result, CPP can be reduced from an increase in ICP, a decrease in blood pressure, or a
combination of both factors. Through the normal regulatory process called pressure
autoregulation, the brain is able to maintain a normal cerebral blood flow (CBF) with a CPP
ranging from 50 to 150 mm Hg. At CPP values less than 50 mm Hg, the brain may not be able
to compensate adequately, and CBF falls passively with CPP. After injury, the ability of the
brain to pressure autoregulate may be absent or impaired, and even with a normal CPP, CBF
can passively follow changes in CPP.
When CPP is within the normal autoregulatory range (50–150 mmHg), this ability of the brain
to pressure autoregulate also affects the response of ICP to a change in CPP [6–8]. When
pressure autoregulation is intact, decreasing CPP results in vasodilation of cerebral vessels,
which allows CBF to remain unchanged. This vasodilation can result in an increase in ICP,
which further perpetuates the decrease in CPP. This response has been called the vasodilatory
cascade. Likewise, an increase in CPP results in vasoconstriction of cerebral vessels and may
reduce ICP. When pressure autoregulation is impaired or absent, ICP decreases and increases
with changes in CPP.
Intracranial hypertension
Causes of intracranial hypertension
The different causes of intracranial hypertension (Box 1) can occur individually or in various
combinations. In primary causes of increased ICP, normalization of ICP depends on rapidly
addressing the underlying brain disorder. In the second group, intracranial hypertension is due
to an extracranial or systemic process that is often remediable [9–11]. The last group is
composed of the causes of increased ICP after a neurosurgical procedure.
Box 1. Causes of intracranial hypertension

Intracranial (primary)
Brain tumor
Trauma (epidural and subdural hematoma, cerebral contusions)
Nontraumatic intracerebral hemorrhage
Ischemic stroke
Hydrocephalus

Idiopathic or benign intracranial hypertension

Other (eg, pseudotumor cerebri, pneumoencephalus, abscesses, cysts)
Extracranial (secondary)
Airway obstruction
Hypoxia or hypercarbia (hypoventilation)
Hypertension (pain/cough) or hypotension (hypovolemia/sedation)
Posture (head rotation)
Hyperpyrexia
Seizures
Drug and metabolic (eg, tetracycline, rofecoxib, divalproex sodium, lead
intoxication)
Others (eg, high-altitude cerebral edema, hepatic failure)
Postoperative
Mass lesion (hematoma) Edema
Increased cerebral blood volume (vasodilation)

Disturbances of CSF
Intracranial hypertension secondary to traumatic brain injury

Special features should be considered in patients with traumatic brain injury (TBI), in which
lesions may be heterogeneous, and several factors often contribute to increase the ICP [12]:
1. Traumatically induced masses: epidural or subdural hematomas, hemorrhagic
contusions, foreign body, and depressed skull fractures
2. Cerebral edema [13]
3. Hyperemia owing to vasomotor paralysis or loss of autoregulation [14]
4. Hypoventilation that leads to hypercarbia with subsequent cerebral vasodilation
5. Hydrocephalus resulting from obstruction of the CSF pathways or its absorption
6. Increased intrathoracic or intra-abdominal pressure as a result of mechanical
ventilation, posturing, agitation, or Valsalva maneuvers
After evacuation of traumatic mass lesions, the most important cause of increased ICP was
thought to be vascular engorgement [14]. Recent studies have suggested that cerebral edema
is the primary cause in most cases [15].
A secondary increase in the ICP often is observed 3 to 10 days after the trauma, principally as
a result of a delayed hematoma formation, such as epidural hematomas, acute subdural
hematoma, and traumatic hemorrhagic contusions with surrounding edema, sometimes
requiring evacuation [16]. Other potential causes of delayed increases in ICP are cerebral
vasospasm [17], hypoventilation, and hyponatremia.
Neurologic intensive care monitoring

Intracranial hypertension is an important cause of secondary injury in patients with acute
neurologic and neurosurgical disorders and typically mandates specific monitoring. Patients

with suspected intracranial hypertension, especially secondary to TBI, should have monitoring
of ICP; monitoring of cerebral oxygen extraction, as with jugular bulb oximetry or brain tissue
PO2, may also be indicated. Brain-injured patients also should have close monitoring of
systemic parameters, including ventilation, oxygenation, electrocardiogram, heart rate, blood

pressure, temperature, blood glucose, and fluid intake and output. Patients should be monitored
routinely with pulse oximetry and capnography to avoid unrecognized hypoxemia and
hypoventilation or hyperventilation. A central venous catheter commonly is needed to help
evaluate volume status, and a Foley catheter is employed for accurate urine output.
Intracranial pressure monitoring

Clinical symptoms of increased ICP, such as headache, nausea, and vomiting, are impossible
to elicit in comatose patients. Papilledema is a reliable sign of intracranial hypertension, but is
uncommon after head injury, even in patients with documented elevated ICP. In a study of
patients with head trauma, 54% of patients had increased ICP, but only 3.5% had papilledema
on fundoscopic examination [18]. Other signs, such as pupillary dilation and decerebrate
posturing, can occur in the absence of intracranial hypertension. CT scan signs of brain
swelling, such as midline shift and compressed basal cisterns, are predictive of increased ICP,
but intracranial hypertension can occur without those findings [19].
Types of monitors
The ventriculostomy catheter is the preferred device for monitoring ICP and the standard
against which all newer monitors are compared [20]. An intraventricular catheter is connected
to an external pressure transducer via fluid-filled tubing. The advantages of the ventriculostomy
are its relatively low cost, the option to use it for therapeutic CSF drainage, and its ability to
recalibrate to minimize errors owing to measurement drift. The disadvantages are difficulties
with insertion into compressed or displaced ventricles, inaccuracies of the pressure
measurements because of obstruction of the fluid column, and the need to maintain the
transducer at a fixed reference point relative to the patient’s head. The system should be
checked for proper functioning at least every 2 to 4 hours, and any time there is a change in
the ICP, neurologic examination, and CSF output. This check should include assessing for the
presence of an adequate waveform, which should have respiratory variations and transmitted
pulse pressure.
When the ventricle cannot be cannulated, other alternatives can be used. Different non–fluid-
coupled devices are available for ICP monitoring and have replaced the subarachnoid bolt. The
microsensor transducer and the fiberoptic transducer are the most widely available. These
transducer-tipped catheters can be inserted in the subdural space or directly into the brain tissue
[21]. The main advantages of these monitors is the ease of insertion, especially in patients with
compressed ventricles; however, none of the transducer-tipped catheters can be reset to zero
after they are inserted into the skull, and they exhibit measurement drift over time [22].
Subdural and epidural monitors for ICP measurements are less accurate compared to
ventriculostomy or parenchymal monitors.
For surgical patients, the ICP monitor may be inserted at the end of the surgical procedure. ICP
monitoring is continued for as long as treatment of intracranial hypertension is required,
typically 3 to 5 days. A secondary increase in ICP may be observed 3 to 10 days after trauma
in 30% of patients with intracranial hypertension [16] secondary to development of delayed
intracerebral hematoma, cerebral vasospasm, or systemic factors such as hypoxia and
hypotension.

Types of intracranial pressure waveforms

The variations seen in the normal tracing of ICP originate from small pulsations transmitted
from the systemic blood pressure to the intracranial cavity. These blood pressure pulsations
are superimposed on slower oscillation caused by the respiratory cycle. In mechanically

ventilated patients, the pressure in the superior vena cava increases during inspiration, which
reduces venous outflow from the cranium, causing an elevation in ICP.
Pathologic waveforms
As the ICP increases, cerebral compliance decreases, arterial pulses become more pronounced,
and venous components disappear. Pathologic waveforms include Lundberg A, B, and C types.
Lundberg A waves or plateau waves are ICP elevations to more than 50 mm Hg lasting 5 to
20 minutes. These waves are accompanied by a simultaneous increase in MAP, but it is not
clearly understood if the change in MAP is cause or effect. Lundberg B waves or pressure
pulses have an amplitude of 50 mm Hg and occur every 30 seconds to 2 minutes. Lundberg C
waves have an amplitude of 20 mm Hg and a frequency of 4 to 8 per minute; they are seen in
the normal ICP waveform, but high-amplitude C waves may be superimposed on plateau waves
[23].
Indications for intracranial pressure monitoring

Monitoring of ICP is an invasive technique and has some associated risks. For a favorable risk-
to-benefit ratio, ICP monitoring is indicated only in patients with significant risk of intracranial
hypertension [12] (Box 2). Patients with TBI who are particularly at risk for developing an
elevated ICP include those with Glasgow Coma Scale of 8 or less after cardiopulmonary
resuscitation and who have an abnormal admission head CT scan. Such abnormalities might
include low-density or high-density lesions, including contusions; epidural, subdural, or
intraparenchymal hematomas; compression of basal cisterns; and edema [24]. Patients who are
able to follow commands have a low risk for developing intracranial hypertension, and serial
neurologic examinations can be followed.
Box 2: Indications for ICP Monitoring

GCS Score: 3–8 (after resuscitation)
1. Abnormal Admission Head CT Scan
a. Hematoma
b. Contusion
c. Edema
d. Herniation
e. Compressed basal cisterns
2. Normal Admission Head CT Scan PLUS 2 or more of the following
a. Age > 40 years
b. Motor posturing
c. Systolic blood pressure < 90 mm Hg
Although CT scan findings are not accurate in determining the actual ICP, the risk of
developing intracranial hypertension can be predicted. Sixty percent of patients with closed
head injury and an abnormal CT scan have intracranial hypertension. Only 13% of patients

with a normal CT scan have elevated ICP except for patients with certain risk factors, including
age greater than 40 years old, systolic blood pressure less than 90 mm Hg, and decerebrate or
decorticate posturing on motor examination. Patients with a normal CT scan have 60% risk of
intracranial hypertension if they have two risk factors and 4% if they have only one risk factor.
Patients with a Glasgow Coma Scale score greater than 8 also might be considered for ICP
monitoring if they require treatment that would not allow serial neurologic examinations, such
as prolonged anesthesia for surgery of multiple injuries or prolonged pharmacologic paralysis
for ventilatory management, or if they require a treatment that might increase ICP, such as
positive end-expiratory pressure (PEEP). Other, less common indications include patients with
multiple systemic injuries with altered level of consciousness and subsequent to removal of an
intracranial mass (eg, hematoma, tumor) [12]. ICP monitoring also must be considered in
nontraumatic conditions in which an intracranial mass lesion is present (eg, cerebral infarction,
spontaneous intracerebral hemorrhage) and has a likelihood of expansion leading to intracranial
hypertension and clinical deterioration. The duration of monitoring is until ICP has been normal
for 24 to 48 hours without ICP therapy.
Complications of intracranial pressure monitoring

The most common complication of ventriculostomy catheter placement is infection with an
incidence of 5% to 14%; colonization of the device is more common than clinical infection
[25]. A study found no significant reduction in infection rate in patients undergoing
prophylactic change of monitors before day 5, compared with those whose catheters were in
place for 5 days or more.[26]. Factors that are not associated with infection are insertion of the
catheter in the neurologic ICU, previous catheter insertion, drainage of CSF, and use of steroids.
In a group of patients with prolonged ventricular drainage of 10 days or more, a non-linear
increase in daily infection rate was observed over the initial 4 days but remained constant
despite prolonged catheter use [27]. Use of antibiotic-coated ventriculostomy catheters has
been shown to reduce the risk of infection from 9.4% to 1.3% [28]. Other complications of
ventriculostomy catheters are hemorrhage with an overall incidence of 1.4%, malfunction,
obstruction, and malposition.
Intracranial pressure treatment measures: brief summary of goals of therapy

1. Maintain ICP at less than 20 to 25 mm Hg.
2. Maintain CPP at greater than 60 mm Hg by maintaining adequate MAP.
3. Avoid factors that aggravate or precipitate elevated ICP.
An overall approach to the management of intracranial hypertension is presented in Fig. 1.
General care to minimize intracranial hypertension

Prevention or treatment of factors that may aggravate or precipitate intracranial hypertension
is a cornerstone of neurologic critical care. Specific factors that may aggravate intracranial
hypertension include obstruction of venous return (head position, agitation), respiratory
problems (airway obstruction, hypoxia, hypercapnia), fever, severe hypertension,
hyponatremia, anemia, and seizures.
Optimizing cerebral venous outflow

To minimize venous outflow resistance and promote displacement of CSF from the intracranial
compartment to the spinal compartment, elevation of the head of the bed and keeping the head
in a neutral position are standards in neurosurgical care. Some authors have advocated keeping
the patient’s head flat to maximize CPP [7]. Other studies have shown a reduction in ICP
without a reduction in either CPP or CBF in most patients with elevation of the head to 30°

[29]. Still other authors have observed that elevation of the head to 30° reduced ICP and
increased CPP, but did not change brain tissue oxygenation [30]. The reduction in ICP afforded
by 15° to 30° of head elevation is probably advantageous and safe for most patients. When
head elevation is used, the pressure transducers for blood pressure and ICP must be zeroed at
the same level (at the level of the foramen of Monro) to assess CPP accurately.
Increased intra-abdominal pressure, as can occur with abdominal compartment syndrome, also
can exacerbate ICP presumably by obstructing cerebral venous outflow. Several case reports
have observed immediate reductions in ICP with decompressive laparotomy in such
circumstances. A retrospective report indicated that even when abdominal compartment
syndrome is not present, abdominal fascial release can reduce effectively ICP that is refractory
to medical treatment [31].
Respiratory failure
Respiratory dysfunction is common in patients with intracranial hypertension, especially when
the cause is head trauma. Hypoxia and hypercapnia can increase ICP dramatically, and
mechanical ventilation can alter cerebral hemodynamics. Optimal respiratory management is
crucial for control of ICP.
Thirty-six percent of comatose head injury patients present with hypoxia and respiratory
dysfunction requiring mechanical ventilation on admission. Pneumonia and pulmonary
insufficiency occur in 42% and 28% as complications during hospitalization. In 227

spontaneously breathing patients with neurologic disorders, most with intracranial
hypertension, North and Jennett found that 60% had breathing abnormalities, including
periodic respirations, tachypnea, and irregular breathing [32]. Periodic breathing was not
correlated, however, with any particular anatomic site of the neurologic injury. Periodic
episodes of hypoventilation can precipitate increased ICP [33]. Controlled ventilation to
maintain a normal PaCO2 can eliminate this cause of intracranial hypertension.
Mechanical ventilation also can have adverse effects on ICP. PEEP, which may be needed to
improve oxygenation, can increase ICP by impeding venous return and increasing cerebral
venous pressure and ICP, and by decreasing blood pressure leading to a reflex increase of
cerebral blood volume. For PEEP to increase cerebral venous pressure to levels that would
increase ICP, the cerebral venous pressure must at least equal the ICP. The higher the ICP, the
higher the PEEP must be to have such a direct hydraulic effect on ICP. The consequences of
PEEP on ICP also depend on lung compliance, and minimal consequences for ICP usually are
observed when lung compliance is low as in patients with acute lung injury [34].
Sedation and analgesia

Agitation and pain may significantly increase blood pressure and ICP. Adequate sedation and
analgesia is an important adjunct treatment. No sedative regimen has clear advantages in this
patient population. In general, benzodiazepines cause a coupled reduction in cerebral metabolic
rate of oxygen (CMRO2) and CBF, with no effect on ICP, whereas the narcotics have no effect
on CMRO2 or CBF, but have been reported to increase ICP in some patients [35]. One
consideration in the choice of sedative should be to minimize effects on blood pressure because
most available agents can decrease blood pressure. Hypovolemia predisposes to hypotensive
side effects and should be treated before administering sedative agents. Selection of shorter
acting agents may have the advantage of allowing brief interruption of sedation to evaluate
neurologic status.

Fever
Fever increases metabolic rate by 10% to 13% per degree Celsius and is a potent vasodilator.
Fever-induced dilation of cerebral vessels can increase CBF and may increase ICP. Fever
during the postinjury period worsens neurologic injury in experimental models of TBI [36]. In
an observational study in patients with TBI, Jones and colleagues [37] found a significant
relationship between fever and a poor neurologic outcome. While a patient is at risk for
intracranial hypertension, fever should be controlled with antipyretics and cooling blankets.
Infectious causes must be sought and treated with appropriate antibiotics when present.
Hypertension
Elevated blood pressure is seen commonly in patients with intracranial hypertension, especially
secondary to head injury, and is characterized by a systolic blood pressure increase greater than
diastolic increase. It is associated with sympathetic hyperactivity [38]. It is unwise to reduce
systemic blood pressure in patients with hypertension associated with untreated intracranial
mass lesions because cerebral perfusion is being maintained by the higher blood pressure. In
the absence of an intracranial mass lesion, the decision to treat systemic hypertension is more
controversial and may need to be individualized for each patient.
When pressure autoregulation is impaired, which is common after TBI, systemic hypertension
may increase CBF and ICP. In addition, elevated blood pressure may exacerbate cerebral
edema and increase the risk of postoperative intracranial hemorrhage.
Systemic hypertension may resolve with sedation. If the decision is made to treat systemic
hypertension, the choice of antihypertensive agent is important. Vasodilating drugs, such as
nitroprusside, nitroglycerin, and nifedipine, can be expected to increase ICP and may
reflexively increase plasma catecholamines, which may be deleterious to the marginally
perfused injured brain. Sympathomimetic-blocking antihypertensive drugs, such as β-blocking
drugs (labetalol, esmolol) or central acting α-receptor agonists (clonidine), are preferred
because they reduce blood pressure without affecting the ICP. Agents with a short half-life
have an advantage when the blood pressure is labile.
Treatment of anemia
Anecdotal cases have been reported of patients with severe anemia presenting with symptoms
of increased ICP and signs of papilledema, which resolve with treatment of the anemia [39].
The mechanism is thought to be related to the marked increase in CBF that is required to
maintain cerebral oxygen delivery when anemia is severe. Although anemia has not been
clearly shown to exacerbate ICP after TBI, a common practice is to maintain hemoglobin
concentration at a minimum of 10 g/dL. In view of a large randomized trial of critically ill
patients that showed better outcome with a more restrictive transfusion threshold of 7 g/dL
[40], the issue of optimal hemoglobin concentration in patients with TBI needs further study.
Prevention of seizures
The risk of seizures after trauma is related to the severity of the brain injury; seizures occur in
15% to 20% of patients with severe head injury. Seizures can increase cerebral metabolic rate
and ICP, but there is no clear relationship between the occurrence of early seizures and a worse
neurologic outcome [41]. In patients with severe TBI, 50% of seizures may be subclinical and
can be detected only with continuous electroencephalographic monitoring [42]. Significant
risk factors for later seizures are brain contusions, subdural hematoma, depressed skull fracture,
penetrating head wound, loss of consciousness or amnesia for more than 1 day, and age 65
years or older.

In a randomized clinical trial, phenytoin reduced the incidence of seizures during the first week
after trauma, but not thereafter [43]. Based on this study, seizure prophylaxis for patients with
severe brain injury is recommended for the first 7 days after injury. Treatment with
anticonvulsants beyond 7 days should be reserved for patients who develop late seizures [44].
Measures for refractory intracranial hypertension

For patients with sustained ICP elevations of greater than 20 to 25 mm Hg, additional measures
are needed to control the ICP. Emergent surgical management should be considered whenever
intracranial hypertension occurs suddenly or is refractory to medical management.
Medical interventions
Heavy sedation and paralysis
Routine paralysis of patients with neurosurgical disorders is not indicated; however,
intracranial hypertension caused by agitation, posturing, or coughing can be prevented by
sedation and nondepolarizing muscle relaxants that do not alter cerebrovascular resistance
[45]. A commonly used regimen is morphine and lorazepam for analgesia/sedation and
cisatracurium or vecuronium as a muscle relaxant, with the dose titrated by twitch response to
stimulation. Although a disadvantage of this therapy is that the neurologic examination cannot
be monitored closely, the sedatives and muscle relaxants can be interrupted once a day, usually
before morning rounds, to allow neurologic assessments.
Major complications of neuromuscular blockade are myopathy, polyneuropathy, and

prolonged neuromuscular blockade. Myopathy is associated with the use of neuromuscular
blocking agents, particularly in combination with corticosteroids [46]. Polyneuropathy has
been observed in patients with sepsis and multiple organ failure. Prolonged neuromuscular
blockade is seen in patients with multiple organ failure especially with kidney and liver
dysfunction. Recommendations to minimize these complications are limiting the use and dose
of neuromuscular blocking agents, train-of-four monitoring, measuring creatine
phosphokinase daily, and stopping the drug daily to evaluate motor response [47].
Hyperosmolar therapy
Mannitol is the most commonly used hyperosmolar agent for the treatment of intracranial
hypertension. More recently, hypertonic saline also has been used in this circumstance. A few
studies have compared the relative effectiveness of these two hyperosmotic agents, but more
work is needed.
Intravenous bolus administration of mannitol lowers the ICP in 1 to 5 minutes with a peak
effect at 20 to 60 minutes. The effect of mannitol on ICP lasts 1.5 to 6 hours, depending on the
clinical condition [48]. Mannitol usually is given as a bolus of 0.25 g/kg to 1 g/kg body weight;
when urgent reduction of ICP is needed, an initial dose of 1 g/kg body weight should be given.
Arterial hypotension (systolic blood pressure < 90 mm Hg ) should be avoided. Two
prospective clinical trials, one in patients with subdural hematoma and the other in patients
who have herniated from diffuse brain swelling, have suggested that a higher dose of mannitol
(1.4 g/kg) may give significantly better results in these extremely critical situations than lower
doses of mannitol [49,50]. When long-term reduction of ICP is needed, 0.25 to 0.5 g/kg can
be repeated every 2 to 6 hours Attention should be paid to replacing fluid that is lost because
of mannitol-induced diuresis, or else intravascular volume depletion results.
Mannitol has rheologic and osmotic effects. Immediately after infusion of mannitol, there is
an expansion of plasma volume and a reduction in hematocrit and in blood viscosity, which
may increase CBF and on balance increase oxygen delivery to the brain. These rheologic effects

of mannitol depend on the status of pressure autoregulation [51]. In patients with intact pressure
autoregulation, infusion of mannitol induces cerebral vasoconstriction, which maintains CBF
constant, and the decrease in ICP is large. In patients with absent pressure autoregulation,
infusion of mannitol increases CBF, and the decrease in ICP is less pronounced. Mannitol also
may improve microcirculatory rheology [50] and has free radical scavenging effects.
The osmotic effect of mannitol increases serum tonicity, which draws edema fluid from
cerebral parenchyma. This process takes 15 to 30 minutes until gradients are established. Serum
osmolarity seems to be optimal when increased to 300 to 320 mOsm and should be kept at less
than 320 mOsm to avoid side effects of therapy, such as hypovolemia, hyperosmolarity, and
renal failure. Mannitol opens the blood-brain barrier, and mannitol that has crossed the blood-
brain barrier may draw fluid into the central nervous system, which can aggravate vasogenic
edema. For this reason, when it is time to stop mannitol, it should be tapered to prevent a
rebound in cerebral edema and ICP. The adverse effects of mannitol are most likely when
mannitol is present in the circulation for extended periods, such as in slow or continuous
infusions or with repeated administration of higher than necessary doses.
Hypertonic saline, given in concentrations ranging from 3% to 23.4%, also creates an osmotic
force to draw water from the interstitial space of the brain parenchyma into the intravascular
compartment in the presence of an intact blood-brain barrier, reducing intracranial volume and
ICP. In some studies, hypertonic saline has been more effective at reducing ICP than mannitol
[52,53]. Hypertonic saline has a clear advantage over mannitol in hypovolemic and hypotensive
patients. Mannitol is relatively contraindicated in hypovolemic patients because of the diuretic
effects, whereas hypertonic saline augments intravascular volume and may increase blood
pressure in addition to decreasing ICP. Hypertonic saline was not associated with improved
neurologic outcomes, however, when given as a prehospital bolus to hypotensive patients with
severe TBI [54]. Adverse effects of hypertonic saline administration include hematologic and
electrolyte abnormalities, such as bleeding secondary to decreased platelet aggregation and
prolonged coagulation times, hypokalemia, and hyperchloremic acidosis [55]. Hyponatremia
should be excluded before administering hypertonic saline to reduce the risk of central pontine
myelinolysis.[56].
Hyperventilation
Hyperventilation decreases PaCO2, which can induce constriction of cerebral arteries by
alkalinizing the CSF. The resulting reduction in cerebral blood volume decreases ICP.
Hyperventilation has limited use in the management of intracranial hypertension, however,
because this effect on ICP is time limited, and because hyperventilation may produce a
sufficient decrease in CBF to induce ischemia.
The vasoconstrictive effect on cerebral arterioles lasts only 11 to 20 hours because the pH of
the CSF rapidly equilibrates to the new PaCO2 level. As the CSF pH equilibrates, the cerebral
arterioles redilate, possibly to a larger caliber than at baseline, and the initial reduction in
cerebral blood volume comes at the cost of a possible rebound phase of increased ICP [57,
58]. For this reason, the most effective use of hyperventilation is acutely to allow time for other,
more definitive treatments to be put into action. When hypocarbia is induced and maintained
for several hours, it should be reversed slowly, over several days, to minimize this rebound
hyperemia [59].
Hyperventilation decreases CBF, but whether this reduction in flow is sufficient to induce
ischemia in injured brain is controversial. One prospective study showed that acutely reducing
PaCO2 from an average of 36 mm Hg to 29 mm Hg reduced global CBF and significantly
increased the volume of brain that was markedly hypoperfused despite improvements in ICP
and CPP [60]. Diringer and coworkers [61] showed similar changes in CBF with moderate

hyperventilation, but did not observe any changes in regional CMRO2 even when CBF was
reduced to less than 10 mL/100 g/min in injured brain tissue, suggesting that energy failure
associated with cerebral ischemia was not occurring.
Although hyperventilation-induced ischemia has not been clearly shown, routine chronic
hyperventilation (to PaCO2 of 20–25 mm Hg) had a detrimental effect on outcome in one
randomized clinical trial [59]. The authors of this study recommended using hyperventilation
only in patients with intracranial hypertension, rather than as a routine in all head-injured
patients. This view is reinforced in TBI guidelines.
Barbiturate coma
Barbiturate coma should only be considered for patients with refractory intracranial
hypertension because of the serious complications associated with high-dose barbiturates, and
because the neurologic examination becomes unavailable for several days [62]. Pentobarbital
is given in a loading dose of 10 mg/kg body weight followed by 5 mg/kg body weight each
hour for 3 doses. The maintenance dose is 1 to 2 mg/kg/h, titrated to a serum level of 30 to 50
μg/mL or until the electroencephalogram shows a burst suppression pattern. Although routine
use of barbiturates in unselected patients has not been consistently effective in reducing
morbidity or mortality after severe head injury [63,64], a randomized multicenter trial showed
that instituting barbiturate coma in patients with refractory intracranial hypertension resulted
in a twofold greater chance of controlling the ICP [65].
The mechanism of ICP reduction by barbiturates is unclear, but likely reflects a coupled
reduction in CBF and CMRO2, with an immediate effect on ICP. Studies by Messeter and
colleagues [66,67] have suggested that the reduction in ICP with barbiturates is closely tied to
the retention of carbon dioxide reactivity by the brain. Complications occurring during
treatment with barbiturate coma include hypotension in 58% of patients, hypokalemia in 82%,
respiratory complications in 76%, infections in 55%, hepatic dysfunction in 87%, and renal
dysfunction in 47% [68]. Hypotension caused by pentobarbital should be treated first with
volume replacement and then with vasopressors if necessary. Experimental studies suggest
that for the treatment of hypotension associated with barbiturate coma, volume resuscitation
may be better than dopamine [69] because dopamine infusion increased cerebral metabolic
requirements and partially offset the beneficial effects of barbiturates on CMRO2.
Hypothermia
Although a multicenter randomized clinical trial of moderate hypothermia in severe TBI did
not show a beneficial effect on neurologic outcome, it was noted that fewer patients randomized
to moderate hypothermia had intracranial hypertension [70]. A pilot randomized clinical trial
of hypothermia in children with TBI produced similar findings—no improvement in neurologic

outcome, but a reduction in ICP during the hypothermia treatment [71]. Although routine
induction of hypothermia is not indicated at present, hypothermia may be an effective
adjunctive treatment for increased ICP refractory to other medical management.
Steroids
Steroids commonly are used for primary and metastastic brain tumors, to decrease vasogenic
cerebral edema. Focal neurologic signs and decreased mental status owing to surrounding
edema typically begin to improve within hours [72]. Increased ICP, when present, decreases
over the following 2 to 5 days, in some cases to normal. The most commonly used regimen is
intravenous dexamethasone, 4 mg every 6 hours. For other neurosurgical disorders, such as
TBI or spontaneous intracerebral hemorrhage, steroids have not been shown to have a benefit
[73,74] and in some studies have had a detrimental effect [75,76].

The CRASH trial [75] is a recently completed, large (>10,000 patients enrolled), placebo-
controlled randomized clinical trial of methylprednisolone for 48 hours in patients with TBI.
Administration of methylprednisolone resulted in a significant increase in the risk of death
from 22.3% to 25.7% (relative risk 1.15, 95% confidence interval 1.07–1.24). This trial
confirmed previous studies and guidelines that routine administration of steroids is not
indicated for patients with TBI.
Surgical interventions
Resection of mass lesions
Intracranial masses producing elevated ICP should be removed when possible. Acute epidural
and subdural hematomas are a hyperacute surgical emergency, especially epidural hematoma
because the bleeding is under arterial pressure. Brain abscess must be drained, and
pneumocephalus must be evacuated if it is under sufficient tension to increase ICP. Surgical
management of spontaneous intracerebral bleeding is controversial [77].
Cerebrospinal fluid drainage

CSF drainage lowers ICP immediately by reducing intracranial volume and more long-term
by allowing edema fluid to drain into the ventricular system. Drainage of even a small volume
of CSF can lower ICP significantly, especially when intracranial compliance is reduced by
injury. This modality can be an important adjunct therapy for lowering ICP. If the brain is
diffusely swollen, the ventricles may collapse, and this modality then has limited utility.
Decompressive craniectomy
The surgical removal of part of the calvaria to create a window in the cranial vault is the most
radical intervention for intracranial hypertension, negating the Monro-Kellie doctrine of fixed
intracranial volume and allowing for herniation of swollen brain through the bone window to
relieve pressure. Decompressive craniectomy has been used to treat uncontrolled intracranial
hypertension of various origins, including cerebral infarction [78], trauma, subarachnoid
hemorrhage, and spontaneous hemorrhage. Patient selection, timing of operation, type of
surgery, and severity of clinical and radiologic brain injury all are factors that determine the
outcome of this procedure.
Sahuquillo and Arikan [79] reviewed the evidence in the literature for studies evaluating the
effectiveness of decompressive craniectomy after TBI. They found only one small randomized
clinical trial in 27 children with TBI [80]. This trial found a reduced risk ratio for death of 0.54
(95% confidence interval 0.17–1.72), and a risk ratio of 0.54 for death, vegetative status, or
severe disability 6 to 12 months after injury (95% confidence interval 0.29–1.07). All of the
available studies in adults are either case series or cohorts with historical controls. These reports
suggest that decompressive craniectomy effectively reduces ICP in most (85%) patients with
intracranial hypertension refractory to conventional medical treatment [81,82]. Brain
oxygenation measured by tissue PO2 and blood flow estimated by middle cerebral artery flow
velocity also are usually improved after decompressive craniectomy [83,84]. Reported
complications include hydrocephalus, hemorrhagic swelling ipsilateral to the craniectomy site,
and subdural hygroma [81]. A case report of paradoxical herniation also has been reported after
a lumbar puncture in a patient with a decompressive craniectomy [85].
There are limited results from randomized trials to confirm or refute the effectiveness of
decompressive craniectomy in adults. Reports suggest, however, that decompressive
craniectomy may be a useful option when maximal medical treatment has failed to control ICP.
There are ongoing randomized controlled trials in TBI (Rescue ICP [86] and DECRAN). In a
pooled analysis of randomized trials in patients with malignant MCA infarction, decompressive

surgery undertaken within 48 h of stroke was associated with reduced mortality and an
increased proportion of patients with a favourable functional outcome [87].
Summary
Effective treatment of intracranial hypertension involves meticulous avoidance of factors that
precipitate or aggravate increased ICP. When ICP becomes elevated, it is important to rule out
new mass lesions that should be surgically evacuated. Medical management of increased ICP
should include sedation, drainage of CSF, and osmotherapy with either mannitol or hypertonic
saline. For intracranial hypertension refractory to initial medical management, barbiturate
coma, hypothermia, or decompressive craniectomy should be considered. Steroids are not
indicated and may be harmful in the treatment of intracranial hypertension resulting from TBI.
Acknowledgements
This article was supported by NIH grant P01-NS38660.
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Fig. 1.
Diagram of diagnosis and treatment of intracranial hypertension.

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Neurol Clin. 2008 May ; 26(2): 521–541.

Management of Intracranial Hypertension

of intracranial hypertension resulting from traumatic brain injury.

Intracranial hypertension is a common neurologic complication in critically ill patients; it is

*Corresponding author. E-mail address: claudiar@bcm.tmc.edu (C.S. Robertson).

Cerebral dynamics overview

Box 1. Causes of intracranial hypertension

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

Idiopathic or benign intracranial hypertension

Increased cerebral blood volume (vasodilation)

Intracranial hypertension secondary to traumatic brain injury

Neurologic intensive care monitoring

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

systemic parameters, including ventilation, oxygenation, electrocardiogram, heart rate, blood

Intracranial pressure monitoring

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

Types of intracranial pressure waveforms

are superimposed on slower oscillation caused by the respiratory cycle. In mechanically

Indications for intracranial pressure monitoring

Box 2: Indications for ICP Monitoring

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

Complications of intracranial pressure monitoring

Intracranial pressure treatment measures: brief summary of goals of therapy

General care to minimize intracranial hypertension

Optimizing cerebral venous outflow

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

insufficiency occur in 42% and 28% as complications during hospitalization. In 227

Sedation and analgesia

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

edema and increase the risk of postoperative intracranial hemorrhage.

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

Measures for refractory intracranial hypertension

before morning rounds, to allow neurologic assessments.

Major complications of neuromuscular blockade are myopathy, polyneuropathy, and

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

of hypothermia in children with TBI produced similar findings—no improvement in neurologic

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

Cerebrospinal fluid drainage

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

hypertension. Neurology 1965;15:622–41. [PubMed: 14306322]

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

J Neurosurg 1994;80:46–50. [PubMed: 8271021]

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

46. [PubMed: 12654358]

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

hyperventilation after severe traumatic brain injury. J Neurosurg 2002;96:103–8. [PubMed:

2005;365:1957–9. [PubMed: 15936423]

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

severe refractory posttraumatic cerebral edema. Neurosurgery 1997;41:84–92. [PubMed: 9218299]

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

Neurol Clin. Author manuscript; available in PMC 2009 May 1.

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